|Dong-Hwan Yun, MD1;Chi-Un Pae, MD, PhD1,2;Antonio Drago, MD3;Laura Mandelli, MD3;Diana De Ronchi, MD3;Ashwin A. Patkar, MD2;In Ho Paik, MD, PhD1;Alessandro Serretti, MD3; and Jung-Jin Kim, MD, PhD1;
1;Department of Psychiatry, Kangnam St. Mary's Hospital, The Catholic University of Korea College of Medicine, Seoul, Korea,
2;Department of Psychiatry and Behavioral Sciences, Duke University Medical Center, Durham, NC, USA,
3;Institute of Psychiatry, University of Bologna, Bologna, Italy
Objective：We previously reported an association between dysbindin gene (DTNBP1) variants and bipolar I disorder (BID). This paper expands upon previous findings suggesting that DTNBP1 variants may play a role in the response to acute mood stabilizer treatment.
Methods：A total of 45 BID patients were treated with antimanic agents (lithium, valproate, or carbamazepine) for an average of 36.52 (±19.87) days. After treatment, the patients were evaluated using the Clinical Global Impression (CGI) scale and the Young Mania Rating Scale (YMRS) and genotyped for their DTNBP1 variants (rs3213207 A/G, rs1011313 C/T, rs2005976 G/A, rs760761 C/T and rs2619522 A/C).
Results：There was no association between the variants investigated and response to mood stabilizer treatment, even after considering possible stratification factors.
Conclusion：Although the small number of subjects is an important limitation in our study, DTNBP1 does not seem to be involved in acute antimanic efficacy.
Pharmacogenetics;Dysbindin;Bipolar disorder;Antimanic agents.